Ca(2+) and Sr(2+) entry pathways activated by pro-inflammatory agonists FMLP, LTB(4) and PAF have been compared to thapsigargin in human neutrophils. 2-APB (10microM) increased Ca(2+) influx and to a greater extent in agonist than in thapsigargin stimulated neutrophils. This action of 2-APB was specific to Ca(2+) because 2-APB did not augment Sr(2+) entry in agonist and thapsigargin stimulated neutrophils. This suggests that Ca(2+) and Sr(2+) entry can be used to discriminate between receptor and non-receptor (store)-operated Ca(2+) influx. Our data show for the first time that Pyr3 whilst partially inhibiting agonist induced Ca(2+) influx almost completely abolished Ca(2+) influx after thapsigargin stimulation.
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